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1.
AIM: To investigate the effect of interleukin-2(IL-2) on the intracellular calcium in electrically stimulated adult rat ventricular myocytes during anoxia and reoxygenation. METHODS: The isolated cardiac ventricular myocytes were exposed to 5 min anoxia followed by 10 min reoxygenation. Chemical anoxia was introduced by Krebs-Henseleit(K-H) solution containing 10-3 mol/L sodium dithionite. The spectrofluorometric method was used to verify intracellular calcium transient with fura-2/AM as calcium fluorescence probe. RESULTS: It was shown that during anoxia, the amplitude of Ca2+ transient was decreased, diastolic [Ca2+]i, time to peak and time to relaxation of Ca2+ transient were increased. All the parameters were got back but did not returned to the pre-anoxia level during reoxygenation. IL-2 at 2×105 U/L administrated during anoxia aggravated the effect of rexoxygenation on [Ca2+]i transient. Pretreatment with a specific κ opioid antagonist, nor-BNI(10-8 mol/L), abolished the effect induced by IL-2 during anoxia on the [Ca2+]i transients, whereas specific δ opioid antagonist, naltrindole(10-6 mol/L), did not cancel the effect. CONCLUSION: It is concluded that administration of IL-2 during anoxia aggravated the effect of reoxygenation on the [Ca2+]i transients of isolated ventricular myocytes, which was mediated by cardiac κ opioid receptor pathway.  相似文献   

2.
AIM and METHODS: To observe the effects of glucose-free and Mg2+-free in the extracellular fluid on the changes of [Ca 2+]i in the cerebro-cortical neurons damaged by 1mmol/L glutamate using laser confocal scanning microscope. RESULTS: Both frequency and amplitude of neuronal calcium oscillation induced by glutamate were lowered in glucose-free and Mg2+-free buffers. The basic [Ca2+]i concentration was lowered in the former case , but it was elevated in the latter case. CONCLUSION: Mg2+-free aggravates [Ca2+]i overload induced by 1mmol/L glutamate ,under certain conditions the glucose-free might resist damage role of glutamate and Mg2+-free.  相似文献   

3.
AIM: To determine whether nuclear Ca2+ is independently regulated from the cytosolic Ca2+ and nuclear Ca2+ oscillation induced by many modulating factors in cultured rat neonatal myocytes and its mechanism. METHODS: Rat neonatal cardiac myocytes were cultured, and fluo-4/AM was loaded as calcium probe. The changes of cytosolic and nuclear Ca2+ were observed by confocal laser microscopy. RESULTS: Calcium fluorescent intensity oscillated slightly in myocardiocytes and the average intensity was much higher in the nucleus than that in the cytosole. Ca2+ oscillation in nucleus and cytosole induced by norepinephrine, isoproperenol, ATP were completely blocked by Ca2+-ATPase antagonist thapsigargin (10-6 mol/L),L-type Ca2+ channel blocker verapermil (500 μmol/L) and KCl (20 mmol/L). Ca2+-ATPase antagonist thapsigargin completely blocked the propagation of Ca2+ waves and simutaneouly induced a temporary Ca2+ increase followed by a magnificient drop and loss of response to norepinephrine. CONCLUSIONS: The results suggested that generation and maintenance of calcium oscillation both in cytosole and nucleus depended on extracellular Ca2+ influx, membrane potential, Ca2+ release and uptake of cytosolic and nuclear calcium stores. The difference between cytosolic calcium and nuclear calcium indicated that calcium regulating system relatively independent of cytosole may exist in nucleus.  相似文献   

4.
AIM: To investigate the changes of cytosolic free calcium concentration([Ca2+]i) and expression of Bcl-2 in HL-60 cells treated by 6F isolated from Pteris semipinnata L.(PSL), and to discuss the relations between calcium ion and cytotoxicity and DNA fragment induction effects of 6F. METHODS: HL-60 cells were used as in vitro model. [Ca2+]i was measured on fluorescent spectrophotometry using Fura-2/AM as Ca2+ indicator. Bcl-2 expressing level was measured by flow cytometry. Tetrazolium salt(MTT) and diphenylamine staining methods were applied for cytotoxicity assay and DNA fragmentation detection, respectively. RESULTS: [Ca2+]i increased obviously in a dose and time dependent manner after treated HL-60 cells with 6F. 6F decreased the expressing level of Bcl-2. Adding 2 mmol/L Ca2+ to the medium, or 1 mmol/L EDTA to chelate Ca2+, or 4 μmol/L calcium ionophore A 23187 to increase the concentration of cytosolic Ca2+, the DNA fragment induction by 6F was not affected, whereas the cytotoxicity of 6F was enhanced. 250 μmol/L Zn2+ attenuated the DNA fragment induction, and the cytotoxicity of 6F against HL-60 cells was enhanced significantly. CONCLUSION: It was speculated that the decreased expressing of Bcl-2 by compound 6F was related to increased [Ca2+]i in HL-60 cells, and DNA fragment induction was possibly catalyzed by Ca2+ - independent DNase.  相似文献   

5.
AIM: To investigate the role of mitochondrial calcium uniporter (MCU) in high glucose(HG)-induced apoptosis of cardiac myocytes. METHODS: Cardiac myocytes were exposed to normal glucose (5.5 mmol/L glucose+ 19.5 mmol/L mannitol), HG (25 mmol/L glucose), or HG combined with 5 μmol/L spermine for 72 h. Mitochondrial free Ca2+ concentration ([Ca2+]m), MCU at mRNA and protein levels, pyruvate dehydrogenase (PDH) activity, mitochondrial membrane potential (Δψm), the levels of ATP and reactive oxygen species (ROS), and apoptosis were determined. RESULTS: The [Ca2+]m, the mRNA and protein levels of MCU, PDH activity, ATP levels, and Δψm were reduced (P<0.05), while ROS content and the protein levels of caspase-9 and caspase-3 were increased in HG group (P<0.05). Adding 5 μmol/L spermine returned these parameters toward control levels (P<0.05). Moreover, apoptosis was reduced by adding spermine and HG treatment (P<0.05). CONCLUSION: HG-induced cardiac myocyte apoptosis may be associated with the decreased MCU expression and activity, abnormal mitochondrial Ca2+ handling, deviant mitochon-drial respiratory chain, and mitochondrial dysfunction.  相似文献   

6.
AIM:To study the effect of salvia miltiorrhiza (SM) on cell contraction and intracellular calcium of enzymatically isolated rat ventricular myocytes during normoxia and anoxia/reoxygenation.METHODS:Contraction and intracel ular calcium were determined with video tracking system and spectrofluorometric method,and the chemical anoxic method was employed. RESULTS:The ±dL/dtmax, dL of cell contraction and the amplitude of [Ca2+]i in the cardiomyocytes following SM treatment were decreased in a dose-dependent manner. During anoxia, the ±dL/dtmax, dL and amplitude of [Ca2+]i were decreased, while the diastolic Ca2+ level was elevated compared with control group. All the contractile parameters and the diastolic Ca2+ level were back toward pretreatment values during reoxygenation, but could not return to control level. After the treatment with SM (3 g/L), ±dL/dtmax and dL of cell contraction and the amplitude of [Ca2+]i were higher and the diastolic Ca2+ level was lower than those in anoxia/reoxygenation group. CONCLUSION:SM antagonized effects of anoxia and reoxygenation on cell contraction and intracellular calcium in isolated ventricular myocytes.  相似文献   

7.
AIM: The changes of myocardial nuclear membrane Ca2+ -ATPase function was investigated in ischemia/reperfusion injury. METHODS: The model of myocardial ischemia/reperfusion injury was established in rats. Myocardial nuclei were purified with sucrose density centrifugation, the activity of Ca2+ -ATPase was measured and calcium uptake was assayed with [45 Ca2+ ] . RESULTS: Plasma levels of malondialdehyde (MDA) and free fatty acid (FFA) in myocardial ischemia/reperfusion injury increased significantly( P<0.01 vs control). Ca2+ -ATPase activity and [45 Ca2+ ] uptake was lower than normal at below 10 μmol/L, while higher at 50 μmol/L. CONCLUSION:These data indicate dysfunction of nuclear menbrane calcium pump and [45 Ca2+ ] uptake function in myocardial ischemia/reperfusion injury.  相似文献   

8.
AIM: To investigate intracellular free calcium ( [Ca2+]i ) alterations in hypothalamus of febrile rabbits induced by endotoxin (ET), and compare with the effect of ET and IL-1β on i in hypothalamic neurocytes from normothermia rabbits. METHOD: The concentration of [Ca2+]i was determined by using spectrofluorometer and fluorescent Ca2+ probe fura-2 /Am. RESULTS: 1. A minute dose of ET (2 ng/mL) induced a significant rise in [Ca2+]i in hypothalamic neurocytes from normothermia rabbits. The rise in [Ca2+]i in hypothalamic neurocytes from febrile rabbits induced by intravenous injection of ET was also observed. 2. In hypothalamic neurocytes from normotheria rabbits, IL-1β failed to affect [Ca2+]i at concentrations of 100, 500, 1 000ng/mL, respectively. CONCLUSION:The action site of low concentration of calcium that plays a regulatory role during fever seems unlikely to be in cytosolic compartment of hypothalamic neurons. The change of [Ca2+]i in hypothalamic neurocytes by ET can not be considered the direct effect of IL-1β.  相似文献   

9.
AIM: To investigate the role of potassium channels in the regulation of intracellular free calcium concentration ( [Ca2+]i) of pulmonary artery smooth muscle cells (PASMCs) in rats. METHODS: The fluorescence Ca2+ indicator Fura-2/AM was used to observe [Ca2+]i of rat PASMCs in normal and chronic hypoxic condition. The influences of potassium channels on PASMCs proliferation were assessed by MTT assay. RESULTS: 1. In normoxic condition, [Ca2+]i was (156.91±8.60) nmol/L, and in hypoxic condition, [Ca2+]i was (294.01±16.81) nmol/L. 2. In normoxic condition, the voltage-dependent K+-channel antagonist 4-aminopyridine (4AP), but not the Ca2+-activated K+-channel antagonist tetraethylammonium (TEA) and the ATP-sensitive K+-channel antagonist glibenclamide (Glib) increased [Ca2+]i. 3. In hypoxic condition, 4AP and TEA caused the rise in [Ca2+]i , but Glib had no effect on [Ca2+]i. 4. MTT assay showed that 4AP increased the value of absorbing light degree (A value) in normoxic and hypoxic condition (0.582±0.062,0.873±0.043,respectively, P＜0.01), TEA increased A value only in hypoxic condition, and Glib had no effect on the proliferation of PASMCs. CONCLUSIONS: KV plays an important role in the regulation of [Ca2+]i and proliferation of PASMCs. KCa serves as distinct responsive roles in the regulation of proliferation of PASMCs in hypoxic condition. KATP has no effect on [Ca2+]i and proliferation of PASMCs in normoxic and hypoxic conditions.  相似文献   

10.
AIM: To investigate the role of reactive oxygen species (ROS) in the regulation of intracellular Ca2+ induced by angiotensin II (Ang II) in the primarily cultured medullary neurons. METHODS: Primarily cultured medullary neurons were prepared from 14-day-old embryos of Sprague-Dawley rats in the study. The identification of medullary neurons was assessed by double-labeling immunofluorescence. To explore the role of ROS, mainly the superoxide (O2·), the O2·generation was measured using the fluorogenic probe dihydroethidium (DHE). To determine intracellular free calcium concentration ([Ca2+]i), the neurons were loaded with the Ca2+-specific dye Fura-2/AM. The cell viability after adding Ang II was also examined using CCK-8 assay. RESULTS: Most of the cultured cells were medullary neurons, more than 80% of which were glutamate positive neurons. Ang II (5 μmol/L) increased the level of ROS within 10 min in the medullary neurons. Ang II at 5 μmol/L induced a significant[Ca2+]i increase in the medullary neurons, and the effect of Ang II occurred rapidly and reached a peak within 20 min after administration. The level of[Ca2+]i started to decline after washout. The Ca2+ elevation induced by Ang II was significantly decreased by apocynin or TEMPOL. No significant difference in the cell viability between control group and 5 μmol/L Ang II treatment group was observed. CONCLUSION: ROS is involved in the regulation of[Ca2+]i induced by Ang II in the primarily cultured medullary neurons, suggesting a potential intracellular signaling mechanism involved in the Ang II-mediated oxidant regulation of central neural control of blood pressure.  相似文献   

11.
AIM:To explore the effect of hypoxia on rapid pacing-induced calcium transient alternations in ventricular myocytes.METHODS:Ventricular myocytes were isolated from the heart of adult SD rats and cultured in serum-free hypoxic fluid to set up an in vitro model of hypoxia-induced cardiac injury. The calcium transient and its alternations were investigated under confocal laser scanning microscope. The mitochondrial function was also examined by WST-8 kit. RESULTS:Under normoxic condition, the ventricular myocytes were claviform. Low frequency of pacing, ranging from 60 to 240 min-1, induced calcium transient, but not calcium transient alternations, which was elicited by the pacing over a threshold frequency of(288 ±27)min-1. Exposure of the ventricular myocytes to hypoxia did not obviously affect the morphology of the cells, but reduced the threshold frequency of pacing to(227±26) min-1(P<0.05). Additionally, exposure of the cells to hypoxia repressed the activity of mitochondrial dehydrogenase from(100.2±8.7)%(control group) to(57.6±7.5)%, which was partially blocked by L-type Ca2+ channel inhibitor. CONCLUSION:Hypoxia facilitates calcium transient alternations induced by rapid pacing, and the calcium transient alternations are involved in the hypoxia-injured mitochondria function.  相似文献   

12.
AIM: To study the relaxation effect of isoliensinine on high K+-induced isolated mouse airway smooth muscle (ASM) and the underlying mechanism. METHODS: The muscle tension transducer was used to detect the effects of isoliensinine on high K+-induced precontraction and Ca2+ influx in ASM. The technique of patch-clamp and calcium imaging system were respectively used to examine the effects of isoliensinine on LVDCC currents and[Ca2+]i of the ASM cells (ASMCs). RESULTS: Isoliensinine significantly relaxed precontracted ASM induced by high K+ in a concentration-dependent manner. The maximum relaxation ratio was(95.3±3.9)% by isoliensinine at 100 μmol/L. In addition, LVDCC currents were measured using the whole-cell patch-clamp technique, which were abolished by isoliensinine. High K+-induced 340/380 nm fluorescence ratio of Fura-2 was 0.63±0.10 in ASMCs, while it decreased to 0.36±0.05 after the addition of isoliensinine (P<0.01). When isoliensinine was added at the peak point of[Ca2+]i, the ratio rapidly decreased from 0.74±0.02 to 0.42±0.05 (P<0.01). Moreover, isoliensinine inhibited high K+-induced Ca2+ influx-mediated contraction of ASM. CONCLUSION: Isoliensinine inhibits LVDCC currents, terminates Ca2+ influx and reduces[Ca2+]i, eventually resulting in relaxation of the ASM, indicating isoliensinine might be a potential bronchodilator.  相似文献   

13.
AIM: To investigate the effects of sodium hydrosulfide (NaHS), a donor of hydrogen sulfide (H2S), on the membrane permeability, intracellular Ca2+ concentration ([Ca2+]i) and the release of IL-1β induced by adenosine triphosphate (ATP) in rat microglia, and to explore the effect of H2S on ATP-P2X purinergic signaling pathway and the molecular mechanism of its neuroprotective effect. METHODS: Rat microglia in logarithmic growth phase were used in the study. The[Ca2+]i was detected by Fura-2/AM staining. Fluorescent dye YO-PRO-1 was used to observe the membrane permeability. Interleukin-1β (IL-1β) was measured by rat IL-1β ELISA kits. RESULTS: The YO-PRO-1 fluorescence intensity was obviously elevated by ATP induction in a dose-dependent manner in the rat microglia, but this effect was counteracted by NaHS pretreatment (P<0.05).[Ca2+]i rapidly increased and then decreased slowly, forming a stable platform for a long time when rat microglia were treated with ATP. Ca2+ spike activity induced by ATP had no change, but the platform disappeared (P<0.05) after NaHS pretreatment. The ATP and LPS together facilitated the release of IL-1β, but the phenomenon was inhibited by NaHS (P<0.05). CONCLUSION: Hydrogen sulfide may decrease the membrane permeability, calcium inflow and IL-1β release in rat microglia activated by high dose of ATP. The cytoprotection of hydrogen sulfide may be mediated by purinergic signaling pathway.  相似文献   

14.
AIM:To investigate different intracellular concentration of Ca2+ in uterine myometrial cells at term and non-term.METHODS:The living cells suspensions were made to measure intracellular Ca2+ concentrations after stainned by calcium fluorescent indicator Fluo-3 AM, then examined by laser scanning confocal microscope (LSCM).RESULTS:Intracelluar Ca2+ showed very stronger red positive signal in myometrial cells at term than that in non-term cells. [Ca2+]i were (35±8.1) nmol/L at non term and (75±7.3) nmol/L at term, which had significant difference compared with each other (P＜0.05).CONCLUSION:Increase in [Ca2+]i in myometrial cells might play a very important role labor.  相似文献   

15.
AIM: To investigate the interaction of Ca2+-sensing proteins, stromal interaction molecule 1 (STIM1) and calcium release-activated calcium channel protein 1 (Orai1), in Ca2+-sensing receptor (CaSR)-mediated extracellular Ca2+ influx and production of nitric oxide (NO). METHODS: Human umbilical vein endothlial cells (HUVECs) were incubated with CaSR agonist spermine [activating store-operated calcium channels (SOC) and receptor-operated calcium channels (ROC)] alone or combined with CaSR negative allosteric modulator Calhex 231+ROC analogue TPA (activating ROC, blocking SOC), protein kinase C (PKC) inhibitor Ro 31-8220, or PKCα/β1 selective inhibitor Go 6976 (activate SOC, blocking ROC). The protein expression of STIM1 and Orai1 was determined by the method of immunofluorescence. The interaction between STIM1 and Orai1 was examined by co-immunoprecipitation. The second to third passages of HUVECs were divided into STIM1 and Orai1 short hairpin RNA group (shSTIM1+shOrai1 group), vehicle-STIM1+vehicle-Orai1 group and control group, and then incubated with the 4 different treatments above. The intracellular Ca2+ concentration ([Ca2+]i) was detected using the fluorescent Ca2+ indicator Fura-2/AM. The production of NO was also determined by DAF-FM DA fluorescent probe. RESULTS: The protein expression of STIM1 and Orai1 was located in the cytoplasm. Compared with control group, the localization of STIM1 and Orai1 in the cytoplasm was reduced after the HUVECs were incubated with Calhex 231+TPA, Ro 31-8220 or Go 6976, and the interaction of STIM1 and Orai1 was decreased significantly. The [Ca2+]i and the net NO fluorescence intensity in shSTIM1+shOrai1 group were significantly reduced after the 4 different treatments (P<0.05). CONCLUSION: STIM1 and Orai1 are components of SOC and ROC in store-and receptor-operated Ca2+ entry and NO generation.  相似文献   

16.
AIM:To study alterations of cardiac sarcoplasmic reticulum (SR) function in vitamin D3-induced calcium overload rats. METHODS: The Ca-overload rat models were prepared by vitamin D3 plus nicotine. Cardiac SR was seperated by centrifuging. The measurement of SR Ca2+uptake and Ca2+ release activities were preformed by the Millimore filtration technique. Specific SR -ryanodine binding capacity was measured by radioligand method. RESULTS: Compared with control,myocardial calcium content in calcium overload rats increased by 78%(P＜0.01), SR Ca2+ uptake and Ca2+ release activities decreased by 64% and 40% respectively(P＜0.01),and in the meantime ,the Ca2+-ATPase activity decreased by 65%(P＜0.01).Maxmum value for -ryanodine binding decreased by 51%(P＜0.01). CONCLUSION:The function of cardiac SR in calcium-overload rats was decreased.  相似文献   

17.
AIM: To study the effects of tetrandrine(Tet) and fructose-1, 6-diphosphate(FDP) on the elevated intrasynaptosomal [Ca2+]i induced by excitatory amino acids(EAA). METHODS: A rapid method for preparing synaptosomes was used, and intrasynaptosomal free calcium([Ca2+]i) was measured by using the fluorescent indicator quin-2. RESULTS: L-glutamate(Glu, 100 μmol/L), aspartate(Asp, 100 μmol·L-1), N-methy1-D-aspartate(100 μmol/L) and Glu(50 μmol/L) plus Asp(50 μmol/L) all elevated intrasynaptosomal [Ca2+]i in a dose-dependent manner. Pretreatment with Tet(10, 30, 60 μmol/L), FDP(15, 30, 75, 150 μmol/L), MK-801(10, 20 μmol/L) and Tet(15, 30 μmol/L) plus FDP(15, 30 μmol/L) all attenuated the increase in intrasynaptosomal [Ca2+]i induced by EAAs mentioned as above in a dose-dependent manner, and the effect of Tet plus FDP was most significant. CONCLUSION: Both Tet and FDP inhibited a rise in intrasynaptosomal [Ca2+]i induced by EAAs, which may be one of mechanisms that Tet and FDP pretect cerebral tissues against ischemia injury.  相似文献   

18.
AIM: To investigate the heterogeneity of basal intracellular free calcium concentration([Ca2+]i) in peritoneal macrophages(PM) and whether it is relative to the reactivity of PM at the single cell level. METHODS:[Ca2+]iimplicated stimulated were measured by fluorescent microscopic imaging system after loading with fluorescent probe fura-2/AM. Superoxide(O2-)produced by single PM was determined by modified NBT test. RESULTS: The values of basal[Ca2+]idetermined in 392 PMs of 7 mice showed normal distribution [(54±24) nmol/L, n=392] with wide range(less than 20 nmol/L to more than 100 nmol/L), among which about 50% were in the range of 40-60 nmol/L. When stimulated with PMA or fMLP,[Ca2+]iwas increased, the peak values were positively correlated with the basal[Ca2+]iin one mouse(PMA stimulated cells: r=0.52, P<0.01, n=58; fMLP stimulated cells:r=0.59, P<0.01, n=44. Both of the experiments were repeated in 3 mice, the results in the other 2 mice were similar). The O2- in PMA stimulated PMs were also positively correlated with the basal i(r=0.42, P<0.01, n=43, repeated in 4 mice, the results in the other 3 mice were similar). CONCLUSION: Basal[Ca2+]iin murine PM is heterogeneous, and the value of basal[Ca2+]iis tightly correlated to the reactivity of PM stimulated by proinflammatory factors.  相似文献   

19.
AIM: To observe the effects of salidroside on intracellular free Ca2+ concentration in cultured rat cardiomyocytes. METHODS: Primarily cultured cardiomyocytes of neonatal rats were divided into control group, different concentrations of salidroside groups and verapamil pretreatment+different concentrations of salidroside groups. The fluorescent intensity of intercellular free calcium concentration ([Ca2+]i) in cultured cardiomyocytes of newborn rats loaded with fluo-3/AM(5 μmol/L) was measured by laser scanning confocal microscopy. RESULTS: Salidroside at concentrations of 15 mg/L, 30 mg/L and 60 mg/L elevated [Ca2+]i in cultured rat cardiomyocytes with the peak values of 574.08±4.65, 591.86±3.64 and 618.66±4.27, respectively (all P<0.01), indicating that the effect of salidroside on the level of [Ca2+]i was dose-dependent. In the presence of verapamil in D-Hanks solution, salidroside also elevated the fluorescent intensity of [Ca2+]i in cardiomyocytes from 357.74±3.13, 387.17±2.37 and 391.43±1.34 to 480.86±3.98, 496.70±3.08 and 522.18±3.19, respectively (all P<0.01). CONCLUSION: Salidroside increases the release of [Ca2+]i from sarcoplasmic reticulum in cultured rat cardiomyocytes.  相似文献   

20.
AIM: To investigate the role of PI3K-IP3R-Ca2+ pathways in cardiomyocyte hypertrophy induced by tumor necrosis factor-α (TNF-α). METHODS: Myocardial cells of neonatal rats were cultured in vitro. The hypertrophic model was induced by TNF-α. The protein content was assayed with Lowry's method. The volumes of the cardiomyocytes were detected by computer photograph analysis system. The protein synthesis was determined by the method of[3H]-leucine incorporation.[Ca2+]i transient was measured by Till image system with cell-loading Fura-2/AM. RESULTS: LY294002, a PI3K inhibitor, significantly suppressed the amplitude elevation of the spontaneous[Ca2+]i transients induced by TNF-α in cultured ventricular myocytes from neonatal rats. The effect was similar to that of LY294002+2-APB (P>0.05), but lower than that in LY294002+ryanodine group (P<0.05). LY294002 significantly reduced the enhancements of protein content,[3H]-leucine incorporation and cell size induced by TNF-α. The effect was similar to that in 2-APB+LY294002 group, but higher than that in 2-APB group and lower than that in ryanodine+LY294002 group. CONCLUSION: TNF-α induces cardiac hypertrophy through PI3K-IP3R-Ca2+ pathways.  相似文献   

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